title: Melatonin attenuates the decrement of dendritic protein MAP-2 immuno-staining in the hippocampal CA1 and CA3 fields of the aging male rat.
abstract: Neuronal death during brain aging results, at least in part, from the disruption of synaptic connectivity caused by oxidative stress. Synaptic elimination might be caused by increased instability of the neuronal processes. In vitro evidence shows that melatonin increases MAP-2 expression, a protein that improves the stability of the dendritic cytoskeleton, opening the possibility that melatonin could prevent synaptic elimination by increasing dendritic stability. One way to begin exploring this issue in vivo is to evaluate whether long-term melatonin treatment changes the intensity of MAP-2 immuno-staining in areas commonly afflicted by aging that are rich in dendritic processes. Accordingly, we evaluated the effects of administering melatonin for 6 or 12 months on the intensity of MAP-2 immuno-staining in the strata oriens and lucidum of the hippocampal CA1 and CA3 fields of aging male rats, through semi-quantitative densitometry. Melatonin treated rats showed a relative increment in the intensity of MAP-2 immuno-staining in both regions after 6 or 12 months of treatment, as compared with age matched control rats. Although melatonin untreated and treated rats showed a decrease of MAP-2 immuno-staining in the hippocampus with increasing age, such decrement was less pronounced following melatonin treatment. These findings were confirmed by qualitative Western blot analyses. The melatonin effect seems specific because MAP-2 staining in the primary somatosensory cortex was not affected by the treatment. Thus, chronic melatonin administration increases MAP-2 immuno-staining and attenuates its decay in the adult aging hippocampus. These results are compatible with the idea that melatonin could improve dendritic stability and thus diminish synaptic elimination in the aging brain.
authors.affiliation: Departamento de Fisiología, División de Investigación, Facultad de Medicina, Universidad Nacional Autónoma de México, México D.F., México City 04510, Mexico. prieto@servidor.unam.mx
authors.forename: Bertha
authors.initials: B
authors.lastname: Prieto-Gómez
authors.forename: Mireya
authors.initials: M
authors.lastname: Velázquez-Paniagua
authors.forename: Leonora Olivos
authors.initials: LO
authors.lastname: Cisneros
authors.forename: Cruz
authors.initials: C
authors.lastname: Reyes-Vázquez
authors.forename: Francisco
authors.initials: F
authors.lastname: Jiménez-Trejo
authors.forename: Miguel Esteban
authors.initials: ME
authors.lastname: Reyes
authors.forename: Julieta
authors.initials: J
authors.lastname: Mendoza-Torreblanca
authors.forename: Gabriel
authors.initials: G
authors.lastname: Gutiérrez-Ospina
mesh_terms: D000375:Aging / Q000502:physiology*; D000818:Animals; D000975:Antioxidants / Q000494:pharmacology*; D015536:Down-Regulation / Q000187:drug effects*; D006624:Hippocampus / Q000033:anatomy & histology / Q000187:drug effects*; D008297:Male; D008550:Melatonin / Q000494:pharmacology*; D008869:Microtubule-Associated Proteins / Q000378:metabolism*; D051381:Rats; D017208:Rats, Wistar; D018709:Statistics, Nonparametric; D013997:Time Factors
chemical_list: D000975:Antioxidants; C489787:MAP2 protein, rat; D008869:Microtubule-Associated Proteins; D008550:Melatonin